Downregulation of miR-96-5p Inhibits mTOR/NF-κb Signaling Pathway via DEPTOR in Allergic Rhinitis
| Autor: | Xin Wei, Jing Zheng, Min Zeng, Jiabin Zhan, Qiu-Ju Huang, Zhi Fu, Lian-Ya Zeng |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Immunology
DEPTOR Proinflammatory cytokine chemistry.chemical_compound Downregulation and upregulation Western blot medicine Humans Immunology and Allergy PI3K/AKT/mTOR pathway Gene knockdown medicine.diagnostic_test TOR Serine-Threonine Kinases Intracellular Signaling Peptides and Proteins NF-kappa B Interleukin NF-κB General Medicine Rhinitis Allergic MicroRNAs Nasal Mucosa Gene Expression Regulation chemistry Cancer research Cytokines RNA Interference Inflammation Mediators Signal Transduction |
| Zdroj: | International Archives of Allergy and Immunology. 182:210-219 |
| ISSN: | 1423-0097 1018-2438 |
| DOI: | 10.1159/000509403 |
| Popis: | Background: This study aims to investigate the regulatory effect of microRNA-96-5p (miR-96-5p) in the pathophysiological process of allergic rhinitis (AR). Methods: Nasal mucosal tissue samples were collected from AR patients and healthy controls. An in vitro AR model was established by stimulating human nasal epithelial cells (HNECs) with interleukin (IL)-13. The expressions of target genes and proteins were measured by qPCR, Western blot, or ELISA. Dual-luciferase reporter assay and pull-down assay were performed to confirm the interaction between miR-96-5p and DEP domain-containing mammalian target of rapamycin-interacting protein (DEPTOR). Results: The level of miR-96-5p was increased while the expression of DEPTOR was decreased in AR patients. The expressions of proinflammatory cytokines were markedly increased and the mammalian target of rapamycin (mTOR)/NF-κB pathway was activated in HNECs following IL-13 stimulation. miR-96-5p downregulation alleviated the stimulated function by IL-13. DEPTOR was the target of miR-96-5p. Knockdown of DEPTOR reversed the function of miR-96-5p inhibitor on IL-13-stimulated HNECs. Conclusions: The current study showed that miR-96-5p and DEPTOR were aberrantly expressed in AR nasal mucosa. miR-96-5p knockdown inhibited the production of inflammatory cytokines and the activation of mTOR/NF-κB pathway via targeting DEPTOR. These findings suggested that miR-96-5p might be used as a diagnostic marker and therapeutic target for the treatment of AR. |
| Databáze: | OpenAIRE |
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